JC viral infection-related cerebellar degeneration as the first manifestation of AIDS.

strated intact cognitive function. A repeat brain MRI showed remarkable cerebellar atrophy without any supratentorial or white matter lesions ( fig. 1 B). Routine serologic tests including serum vitamin B12 level, folate level and liver enzymes were normal. Cerebrospinal fluid (CSF) analysis was unremarkable. Genetic studies for spinocerebellar ataxia (types 1, 2, 3, 6 and 7) and Friedreich ataxia were negative. Paraneoplastic markers including antiHu, anti-Yo and anti-Purkinje-cell antibodies were also negative. CSF revealed no antibodies for cytomegalovirus, herpes simplex, varicella-zoster or Toxoplasma gondii . Anti-HIV antibody and HIV antigen were positive in both serum and CSF. This was later confirmed by Western blot testing. The absolute CD4+ lymphocyte count was 1 cell/mm 3 , 205 CD8+ cells/ mm 3 , and the plasma HIV viral load was 410,000 copies/ml. One month after admission, JC viral DNA was detected in CSF by polymerase chain reaction. A highly active antiretroviral treatment (HAART) regimen, composed of zidovudine, lamivudine, lopinavir and ritonavir, was initiated and maintained. The HIV viral load was significantly reduced to 25 copies/ml at 3 months, and less than 25 copies/ml at 6 months after treatment. The absolute CD4+ and CD8+ lymphocyte counts were increased to 35 and 1,305 cells/mm 3 at 3 months, and 57 and 962 cells/mm 3 at 6 months after HAART, reDear Sir, Primary cerebellar degeneration is rarely associated with human immunodeficiency virus type 1 (HIV) infection [1] . Since the cerebellum is not immune to the ravages of HIV infection [1] , its underlying mechanism is still obscure. Recently, the human polyomavirus JC (JCV), a wellknown causative agent of progressive multifocal leukoencephalopathy (PML) in immunosuppressed individuals, was reported to produce granule cell damage in a patient with acquired immune deficiency syndrome (AIDS) [2, 3] . Here, we introduce a patient with AIDS who presented with subacute onset of progressive cerebellar degeneration and central nervous system (CNS) infection with JCV.